PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
27034723-5	2016	In the treatment of diabetic ED, a traditionally difficult-to-treat population, 100 mg mirodenafil has been reported to offer favorable efficacy (with improvements in the IIEF-EF scores, and positive responses to the SEP2 and the SEP3: 9.3 points, 36.1% and 61.8%, respectively) and tolerability (mild adverse effects of less than 19.6%), which are comparable with results from clinical studies on other PDE5Is.	mirodenafil	87-98	septin 6	Homo sapiens	217-221
33987996-8	2022	SEP2 and SEP3 were increased in both mirodenafil groups; however, the increase was not statistically significant for SEP2.	mirodenafil	37-48	septin 8	Homo sapiens	0-4
33987996-8	2022	SEP2 and SEP3 were increased in both mirodenafil groups; however, the increase was not statistically significant for SEP2.	mirodenafil	37-48	septin 3	Homo sapiens	9-13
26919966-1	2016	OBJECTIVE: To evaluate the distribution of a daily phosphodiesterase type 5 inhibitor dose (mirodenafil) in rat plasma and bladder and prostate tissue in a model of atherosclerosis-induced chronic pelvic ischemia.	mirodenafil	92-103	phosphodiesterase 5A	Rattus norvegicus	51-75
27034723-3	2016	Mirodenafil, a second-generation PDE5I, has biochemical profiles such as high affinity for PDE5 and high selectivity for PDE5 over other PDE isoforms, compared to other existing PDE5Is such as sildenafil, vardenafil and tadalafil.	mirodenafil	0-11	phosphodiesterase 5A	Homo sapiens	33-37
27034723-3	2016	Mirodenafil, a second-generation PDE5I, has biochemical profiles such as high affinity for PDE5 and high selectivity for PDE5 over other PDE isoforms, compared to other existing PDE5Is such as sildenafil, vardenafil and tadalafil.	mirodenafil	0-11	phosphodiesterase 5A	Homo sapiens	91-95
27034723-3	2016	Mirodenafil, a second-generation PDE5I, has biochemical profiles such as high affinity for PDE5 and high selectivity for PDE5 over other PDE isoforms, compared to other existing PDE5Is such as sildenafil, vardenafil and tadalafil.	mirodenafil	0-11	phosphodiesterase 5A	Homo sapiens	91-95
27034723-5	2016	In the treatment of diabetic ED, a traditionally difficult-to-treat population, 100 mg mirodenafil has been reported to offer favorable efficacy (with improvements in the IIEF-EF scores, and positive responses to the SEP2 and the SEP3: 9.3 points, 36.1% and 61.8%, respectively) and tolerability (mild adverse effects of less than 19.6%), which are comparable with results from clinical studies on other PDE5Is.	mirodenafil	87-98	septin 3	Homo sapiens	230-234
24872948-3	2014	Mirodenafil is a newly developed pyrrolopyrimidinone compound, which is a potent, reversible, and selective oral PDE5 inhibitor.	mirodenafil	0-11	phosphodiesterase 5A	Homo sapiens	113-117
23700501-10	2013	The two groups treated with mirodenafil, however, showed decreased connexin 43 staining compared with the untreated BOO group.	mirodenafil	28-39	gap junction protein, alpha 1	Rattus norvegicus	67-78
23700501-12	2013	Decreasing bladder overactivity by mirodenafil may be related to intracellular communication mechanisms involving connexin 43.	mirodenafil	35-46	gap junction protein, alpha 1	Rattus norvegicus	114-125
23006442-8	2012	The geometric mean (95% CI) of the terminal half-life (t1/2beta) and the apparent clearance (CL/F) values of mirodenafil were 2.2 (1.4 - 3.4) h and 127.2 (95.1 - 170.2) l/h in the volunteer patients, and 3.0 (2.1 - 4.4) h and 136.1 (74.4 - 249.2) l/h in the healthy volunteers, respectively.	mirodenafil	109-120	interleukin 1 receptor like 1	Homo sapiens	55-63
21460862-7	2011	We found reports on five kinds of PDE-5 inhibitors for the management of ED: sildenafil, vardenafil, tadalafil, udenafil and mirodenafil.	mirodenafil	125-136	phosphodiesterase 5A	Homo sapiens	34-39
20626604-1	2010	INTRODUCTION: Mirodenafil is a newly developed selective phosphodiesterase type 5 (PDE5) inhibitor for the treatment of erectile dysfunction (ED).	mirodenafil	14-25	phosphodiesterase 5A	Homo sapiens	57-81
20626604-8	2010	Differences between the mirodenafil and placebo groups were significant in the SEP2 (82.0% vs. 55.2%, P = 0.0003), SEP3 (68.9% vs. 22.3%, P < 0.0001).	mirodenafil	24-35	septin 3	Homo sapiens	115-119
21585174-7	2011	Among the other PDE5 inhibitors under development we report mirodenafil, lodenafil carbonate, avalafil and SLx-2101 It is likely that in the future molecules that act on pathways other than the one of NO/cGMP will be available.	mirodenafil	60-71	phosphodiesterase 5A	Homo sapiens	16-20
20649936-8	2010	The mirodenafil group also demonstrated significantly greater improvement in scores of IIEF Q3 and Q4, other four domains of IIEF, SEP2, SEP3, and LSC along with percentages of patients responding positively to GAQ compared with the placebo group.	mirodenafil	4-15	septin 6	Homo sapiens	131-135
20649936-8	2010	The mirodenafil group also demonstrated significantly greater improvement in scores of IIEF Q3 and Q4, other four domains of IIEF, SEP2, SEP3, and LSC along with percentages of patients responding positively to GAQ compared with the placebo group.	mirodenafil	4-15	septin 3	Homo sapiens	137-141
20626604-1	2010	INTRODUCTION: Mirodenafil is a newly developed selective phosphodiesterase type 5 (PDE5) inhibitor for the treatment of erectile dysfunction (ED).	mirodenafil	14-25	phosphodiesterase 5A	Homo sapiens	83-87
20626604-8	2010	Differences between the mirodenafil and placebo groups were significant in the SEP2 (82.0% vs. 55.2%, P = 0.0003), SEP3 (68.9% vs. 22.3%, P < 0.0001).	mirodenafil	24-35	septin 6	Homo sapiens	79-83
19929308-2	2010	This may be explained by the significantly faster hepatic CL(int) of mirodenafil, owing to increased hepatic CYP1A, CYP2B1/2, CYP2D, and CYP3A expression, and a faster hepatic blood flow rate, compared with control values.	mirodenafil	69-80	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	116-122
19929308-2	2010	This may be explained by the significantly faster hepatic CL(int) of mirodenafil, owing to increased hepatic CYP1A, CYP2B1/2, CYP2D, and CYP3A expression, and a faster hepatic blood flow rate, compared with control values.	mirodenafil	69-80	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	137-142
20110038-3	2009	OBJECTIVE: The aim of this study was to investigate the effects of a potent inhibitor (ketoconazole) and inducer (rifampicin) of the CYP3A4 isozyme on the pharmacokinetics of mirodenafil to meet the regulatory requirements for the marketing of mirodenafil in Korea.	mirodenafil	175-186	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	133-139
20456834-1	2010	PURPOSE: This study was performed to find which types of hepatic CYP isoforms are responsible for the metabolism of mirodenafil (a new erectogenic) and one of its metabolite, SK3541, using various hepatic CYP inducers and inhibitors in rats.	mirodenafil	116-127	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	65-68
20456834-2	2010	METHODS: Mirodenafil at a dose of 20 mg/kg was administered intravenously to control rats and rats pretreated with various CYP inducers and inhibitors.	mirodenafil	9-20	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	123-126
20456834-8	2010	CONCLUSIONS: The above data suggest that hepatic CYP1A1/2, 2B1/2, 2D subfamily, and 3A1/2 are involved in the metabolism of both mirodenafil and SK3541 in rats.	mirodenafil	129-140	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	49-55
20110038-3	2009	OBJECTIVE: The aim of this study was to investigate the effects of a potent inhibitor (ketoconazole) and inducer (rifampicin) of the CYP3A4 isozyme on the pharmacokinetics of mirodenafil to meet the regulatory requirements for the marketing of mirodenafil in Korea.	mirodenafil	244-255	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	133-139
18197727-5	2008	In addition, several new PDE5 inhibitors are candidates to enter the market in forthcoming years (avanafil, udenafil, SLx-2101, mirodenafil [SK3530]).	mirodenafil	128-139	phosphodiesterase 5A	Homo sapiens	25-29
19814864-5	2009	KEY FINDINGS: After interavenous administration of mirodenafil to U-ARF rats, the total area under the concentration-time curve (AUC) of mirodenafil was significantly smaller (36.5% decrease) than controls, possibly due to the significantly faster non-renal clearance (66.1% increase; because of increase in the protein expression of hepatic CYP3A1) than controls.	mirodenafil	51-62	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	342-348
19814864-5	2009	KEY FINDINGS: After interavenous administration of mirodenafil to U-ARF rats, the total area under the concentration-time curve (AUC) of mirodenafil was significantly smaller (36.5% decrease) than controls, possibly due to the significantly faster non-renal clearance (66.1% increase; because of increase in the protein expression of hepatic CYP3A1) than controls.	mirodenafil	137-148	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	342-348
19814864-6	2009	After the oral administration of mirodenafil to U-ARF rats, the AUC of mirodenafil was also significantly smaller (47.8% decrease) due to the increase in the protein expression of hepatic CYP3A1 and intestinal CYP1A1 and 3A1/2 compared with controls.	mirodenafil	33-44	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	188-194
19814864-6	2009	After the oral administration of mirodenafil to U-ARF rats, the AUC of mirodenafil was also significantly smaller (47.8% decrease) due to the increase in the protein expression of hepatic CYP3A1 and intestinal CYP1A1 and 3A1/2 compared with controls.	mirodenafil	33-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	210-216
19814864-6	2009	After the oral administration of mirodenafil to U-ARF rats, the AUC of mirodenafil was also significantly smaller (47.8% decrease) due to the increase in the protein expression of hepatic CYP3A1 and intestinal CYP1A1 and 3A1/2 compared with controls.	mirodenafil	71-82	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	188-194
19814864-6	2009	After the oral administration of mirodenafil to U-ARF rats, the AUC of mirodenafil was also significantly smaller (47.8% decrease) due to the increase in the protein expression of hepatic CYP3A1 and intestinal CYP1A1 and 3A1/2 compared with controls.	mirodenafil	71-82	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	210-216
19695390-1	2009	BACKGROUND: Mirodenafil is a phosphodiesterase type 5 (PDE-5) inhibitor developed for the treatment of erectile dysfunction.	mirodenafil	12-23	phosphodiesterase 5A	Homo sapiens	29-53
19695390-1	2009	BACKGROUND: Mirodenafil is a phosphodiesterase type 5 (PDE-5) inhibitor developed for the treatment of erectile dysfunction.	mirodenafil	12-23	phosphodiesterase 5A	Homo sapiens	55-60
18098061-2	2008	CYP3A4 was identified as the major enzyme and CYP2C8 as a minor enzyme responsible for mirodenafil N-dealkylation based on correlation analysis, inhibition studies, and cDNA-expressed CYP enzyme activities.	mirodenafil	87-98	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	46-52
18098061-0	2008	Identification of cytochrome P450 enzymes responsible for N -dealkylation of a new oral erectogenic, mirodenafil.	mirodenafil	101-112	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	18-33
18098061-2	2008	CYP3A4 was identified as the major enzyme and CYP2C8 as a minor enzyme responsible for mirodenafil N-dealkylation based on correlation analysis, inhibition studies, and cDNA-expressed CYP enzyme activities.	mirodenafil	87-98	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-3
18098061-1	2008	The purpose of this paper is to characterize the cytochrome P450 (CYP) enzymes involved in the metabolism of a new oral erectogenic, mirodenafil, to a major circulating active metabolite, N-dehydroxyethyl-mirodenafil, and to investigate the inhibitory potential of mirodenafil on seven CYP enzymes in human liver microsomes.	mirodenafil	133-144	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	49-64
18098061-3	2008	Plasma concentrations of mirodenafil and its N-dealkylated metabolite could therefore change with co-administration of known CYP3A4 inducers or inhibitors.	mirodenafil	25-36	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	125-131
18098061-1	2008	The purpose of this paper is to characterize the cytochrome P450 (CYP) enzymes involved in the metabolism of a new oral erectogenic, mirodenafil, to a major circulating active metabolite, N-dehydroxyethyl-mirodenafil, and to investigate the inhibitory potential of mirodenafil on seven CYP enzymes in human liver microsomes.	mirodenafil	133-144	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	66-69
18098061-1	2008	The purpose of this paper is to characterize the cytochrome P450 (CYP) enzymes involved in the metabolism of a new oral erectogenic, mirodenafil, to a major circulating active metabolite, N-dehydroxyethyl-mirodenafil, and to investigate the inhibitory potential of mirodenafil on seven CYP enzymes in human liver microsomes.	mirodenafil	133-144	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	286-289
18098061-4	2008	Mirodenafil inhibited CYP3A4, CYP2C19 and CYP2D6 activities with IC50 values of 15.6, 38.2 and 77.0 microM, respectively, in human liver microsomes.	mirodenafil	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	22-28
18098061-1	2008	The purpose of this paper is to characterize the cytochrome P450 (CYP) enzymes involved in the metabolism of a new oral erectogenic, mirodenafil, to a major circulating active metabolite, N-dehydroxyethyl-mirodenafil, and to investigate the inhibitory potential of mirodenafil on seven CYP enzymes in human liver microsomes.	mirodenafil	205-216	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	49-64
18098061-4	2008	Mirodenafil inhibited CYP3A4, CYP2C19 and CYP2D6 activities with IC50 values of 15.6, 38.2 and 77.0 microM, respectively, in human liver microsomes.	mirodenafil	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
18098061-1	2008	The purpose of this paper is to characterize the cytochrome P450 (CYP) enzymes involved in the metabolism of a new oral erectogenic, mirodenafil, to a major circulating active metabolite, N-dehydroxyethyl-mirodenafil, and to investigate the inhibitory potential of mirodenafil on seven CYP enzymes in human liver microsomes.	mirodenafil	205-216	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	66-69
18098061-1	2008	The purpose of this paper is to characterize the cytochrome P450 (CYP) enzymes involved in the metabolism of a new oral erectogenic, mirodenafil, to a major circulating active metabolite, N-dehydroxyethyl-mirodenafil, and to investigate the inhibitory potential of mirodenafil on seven CYP enzymes in human liver microsomes.	mirodenafil	205-216	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	286-289
18098061-4	2008	Mirodenafil inhibited CYP3A4, CYP2C19 and CYP2D6 activities with IC50 values of 15.6, 38.2 and 77.0 microM, respectively, in human liver microsomes.	mirodenafil	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	42-48
18098061-2	2008	CYP3A4 was identified as the major enzyme and CYP2C8 as a minor enzyme responsible for mirodenafil N-dealkylation based on correlation analysis, inhibition studies, and cDNA-expressed CYP enzyme activities.	mirodenafil	87-98	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6